Current Insight on the Pathophysiology of Vasovagal Syncope: What Have We Learned?

Abstract

The mechanisms leading to the development of the vasovagal response have fascinated physiologists and physicians for centuries. The first description of a vasodepressor response may have been inadvertently provided by John Hunter (1728–1729) when he wrote: “I bled a lady but she fainted and while she continued in the fit the colour of the blood that came from the vein was a fine scarlet. The circulation was very languid [1]:” Hunter may have described the effects of vasodilatation during a vasovagal syncopal episode provoked by controlled hypovolemia [2, 3]. Not until this century, did Sir Thomas Lewis [4] provide a cardinal observation in the mid 1920s when he demonstrated that prevention of bradycardia with atropine did not reverse the blood pressure fall without affecting the onset of syncope. This finding led Lewis to hypothesize that a peripheral mechanism that rested in the blood vessels was essential for the development of the vasodepressor response. This chapter will focus primarily on recent evidence obtained from studies that have assessed heart rate variability, arterial and cardiopulmonary baroreflex sensitivity, and muscle sympathetic nerve traffic in subjects with vasovagal syncope (VVS).